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Involvement of abnormally‐activated CD44+ cells migrating from the iris to the center of the cornea in Fuchs Endothelial Corneal Dystrophy
Author(s) -
He Z.,
Thuret G.,
Jun A.S.,
Muraine M.,
Kallay L.,
Toubeau D.,
Pereira S.,
Bergandi F.,
Gain P.
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2016.0373
Subject(s) - corneal endothelium , endothelium , cornea , extracellular matrix , pathology , cd44 , population , biology , microbiology and biotechnology , ophthalmology , medicine , cell , genetics , environmental health , endocrinology
Purpose Normal regeneration of the adult corneal endothelium and cellular mechanisms involved in Fuchs endothelial corneal dystrophy (FECD) remain poorly understood. Aim: to present original observations establishing common ground between both mechanisms in order to open new perspectives in their understanding. Methods 30 corneal buttons of FECD, and of other corneal diseases, 40 healthy whole corneas, and 6 whole corneas with early stages of FECD were used. Mean donor age was 72 years. Immunostaining on flat mounted corneas highlighted the expression of corneal endothelial cell (CEC), of stem cell, and of extracellular matrix (ECM) markers. Results The central endothelium of FECD and the extreme peripheral endothelium of healthy corneas shared common features: a weak expression of CEC markers (Na+/K+ ATPase, ZO‐1, COX IV, NCAM, CD166), expression of stem cells markers (nestin, c‐myc, telomerase, CD44), similar characteristics in Descemet membrane (Guttae and Hassal‐Henle bodies, high expression in col I, IV and V). An anatomical continuity and cell migration from the iris root, through TM, until the extreme peripheral endothelium was highlighted using col I and CD44. Similar CD44+ cells, and pseudo guttae were also observed in the central endothelium of corneal buttons with irido‐corneal synechiae. Conclusions Results suggest that a population of iris‐derived CD44+ cells migrate through the TM to the extreme periphery to constitute a source for endothelium regeneration in healthy corneas; their abnormally‐activated migration toward the center might cause FECD.